Cell death is classified from morphological change into necrosis that whole cells are swelled by cell membrane degeneration and die out, and apoptosis that whole cells reduce the sizes to change the nuclear structure and to fragmentize DNA into ladders and die out (Kerr and Harrnon, Apoptosis: The molecular Basis of Cell Death, Tomei and Cope (Eds), pp5-29 (1991), Cold Spring Harbor Laboratory Press). It has become clear that the apoptosis is greatly involved in pathology suffering from many diseases, and there is possibility of new treatment by controlling inappropriate apoptosis (Thompson, Science, Vol. 267, pp 1456-1462 (1995)).
Several lines of evidence suggest that neuronal cell death in neuro degenerative disorders occurs by apoptosis (Alzheimer disease, Parkinson disease, Huntington chorea, amyotrophic lateral sclerosis and the like) (Su et al., Neuro Report, Vol. 5, pp 2529-2533 (1994); Yoshiyama et al., Acta Neuropathologica, Vol. 88, pp 207-211 (1994); Lassman et al., Acta Neuropathologica, Vol. 89, pp 35-41 (1995); Smale et al., Experimental Neurology, Vol. 133, pp 225-230 (1995); Dragunow et al., Neuro Report, Vol. 6, pp 1053-1057 (1995); Portera-Cailliau et al., Journal of Neuroscience, Vol. 15, pp 3775-3787 (1995); Cotman and Anderson, Molecular Neurobiology, Vol. 10, pp 19-45 (1995); Bredesen, Annals of Neurology, Vol. 38, pp 839-851 (1995)). In addition, apoptosis has been suggested to play a role in delayed neuronal death of Mongolian gerbil following transitant ischemia (Nitatori et al., Journal of Neuroscience, Vol. 15, pp 1001-1011 (1995)). As some agents for inhibiting neuronal apoptotic cell death, protein and RNA synthesis inhibitors can be exemplified. However, specificity of these inhibitors for advanced drug development is questionable. Further, a product of Bcl-2 gene and a protein factor such as a neurotropic factor have problems because these are not safely and effectively administered in vivo, so that these are not practically used. Therefore, therapeutic method for the control of neuronal cell death in neurodegenerative disorders has not been established. Hitherto, many isoquinoline derivatives are known, especially, a compound binding an alkyl group via an sulfur atom at a 5-position of isoquinoline (Euerby, Mervin R. and Waigh, Roger D., J. Chem. Soc. Chem. Commun., Vol. 2, 127-128 (1984)). However, a compound binding an aromatic ring via a sulfur atom at a 5-position of isoquinoline has not been known.